Diarrhea metabolic alkalosis

Patients with a jejunostomy are at risk of hypokalemia as weU, so potassium levels must be monitored closely for supplementation. Other patients at risk for potassium depletion include individuals with long-term sodium depletion, magnesium deficiency, or excessive loss from diarrhea. Metabolic alkalosis, which may occur when a patient becomes dehydrated, accelerates the renal excretion of potassium, as all hydrogen ions are conserved in an attempt to correct the acid-base disorder. As bicarbonate ions are excreted renaUy, potassium is taken with them to maintain osmotic balance. 

Oral Treatment of hypokalemia in the following conditions With or without metabolic alkalosis digitalis intoxication familial periodic paralysis diabetic acidosis diarrhea and vomiting surgical conditions accompanied by nitrogen loss, vomiting, suction drainage, diarrhea, and increased urinary excretion of potassium certain cases of uremia hyperadrenalism starvation and debilitation corticosteroid or diuretic therapy. 

Hypokalemia is common in the patient with liver failure who has normal renal function. Poor nutritional intake and vomiting may initiate this disorder. Severe vomiting may lead to volume contraction metabolic alkalosis, with increased renal excretion of potassium. Secondary hyperaldosteronism, seen in the liver failure patient with intravascular depletion, also increases renal excretion of potassium. Loop diuretic therapy causes increased renal excretion of potassium, whereas diarrhea from lactulose therapy increases fecal excretion of potassium. All these conditions can lead to profound hypokalemia. Therefore, potassium requirements in the liver failure patient receiving specialized nutritional support often are increased substantially. 

A deficiency of salt (sodium) may cause reduced growth, loss of appetite, loss of body weight due to loss of body water, reduced milk production of lactating mothers, muscle cramps, nausea, diarrhea, and headache. In cases of prolonged or severe vomiting, or indiscreet use of diuretics, chloride losses may exceed that of sodium—resulting in a state of metabolic alkalosis. To restore the acid-base balance of the body, adequate chloride must be provided. 

Prolonged use or overdose may result in electrolyte or metabolic disturbances (such as hypokalemia, hypocalcemia, and metabolic acidosis or alkalosis), as well as persistent diarrhea, vomiting, muscle weakness, malabsorption, and weight loss. 

Contraindications Excessive chloride loss due to diarrhea, diuretics, GI suctioning, or vomiting hypocalcemia metabolic or respiratory alkalosis, HTN, CHF... 

Acute toxicity manifests primarily in the CNS, cardiovascular system, and gastrointestinal system. CNS signs include restlessness, tremor, nervousness, headache, insomnia, tinnitus, confusion, delirium, psychosis, and seizures. Cardiac manifestations of overdose include sinus tachycardia, various dysrhythmias, asystole, and cardiovascular collapse. Other findings include tachypnea, nausea, vomiting, hematemesis, diarrhea, and fever. Case reports also include rhabdomyolysis and pulmonary edema. Laboratory findings include metabolic acidosis, respiratory alkalosis, ketosis, hypokalemia, and hyperglycemia. The estimated lethal dose in adults is 150-200 mg kg whereas doses of 10-15mgkg ... 

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